kaolinite and Nerve-Degeneration

Whether or not neuron death plays a major role in pathophysiology during hydrocephalus is not well known. The goals of this study were to determine if neural degeneration occurred during hydrocephalus, and to determine if neuron tolerance developed during this pathophysiologic procedure.Neural damage as visualized by a sensitive staining technique, silver impregnation, was observed in three experimental groups: (1) adult hydrocephalic rats induced by kaolin injection into the cisterna magna, (2) adult rats with chronic hydrocephalus for 10 weeks subjected to acute forebrain ischemia induced by four-vessel occlusion, and (3) adult rats without hydrocephalus subjected to acute forebrain ischemia. The magnitude of hydrocephalus was also evaluated during this time. In mild or moderate hydrocephalus, little cell death was found. In severe hydrocephalus, axon and neuropil degeneration was extensively distributed, but cell death was still rarely observed. Although some neuron degeneration was found after acute forebrain ischemia in hydrocephalic rats, the extensive cell death in cortical layers III and V, and in hippocampal areas CA1 and CA4 that is commonly observed in the ischemic brain without hydrocephalus, was not seen. This study suggests that neuron death was not a major pathological change in the brain during hydrocephalus, with cerebral ventricles being enlarged during the development of hydrocephalus. Less neuron death in hydrocephalic rats after acute forebrain ischemia suggests that neuronal tolerance to ischemia occurs during hydrocephalus.

Topics: Animals; Axons; Brain; Brain Ischemia; Cell Survival; Cerebral Cortex; Cerebral Ventricles; Dendrites; Hippocampus; Hydrocephalus; Kaolin; Nerve Degeneration; Neurons; Rats; Rats, Sprague-Dawley; Silver Staining

Hydrosyringomyelia was produced experimentally by the injection of kaolin into the cisterna magna of the rabbit, and the ultrastructural changes of the spinal cord surrounding the syrinx were investigated 2, 4, and 6 weeks after injection by transmission electron microscopy. The ependyma at the ventral part of the central canal was flat and stretched, whereas, in the dorsal part, it was split, and the syrinx extended through the dorsal median plane in most animals. Extracellular edema was found in the subependymal white matter and in and around the posterior median septum. Many nerve fibers surrounding the syrinx were in varying stages of axonal degeneration. Myelin sheaths were split, thinned, and completely lost in many nerve fibers. In some fibers, the axons were totally lost, leaving the myelin sheaths as empty tubes. Astrocytic processes containing a large number of glial filaments covered the nerve fibers adjacent to the syrinx and partially replaced the edematous area. The perivascular spaces were enlarged, especially near the syrinx and in the dorsal white matter. Oligodendrocytes remained undamaged, and the remyelination by oligodendrocytic processes was seen on some denuded axons. Sometimes, this further remyelination was abortive, especially where the edema was severe. The ultrastructural changes of the neural tissue and their sequences were identical, in most respects, to those of hydrocephalus and noncommunicating syringomyelia. The oligodendrocytic remyelination with ongoing demyelination found in this model has many similarities to those in experimental hydrocephalus.

Topics: Animals; Cisterna Magna; Ependyma; Injections, Spinal; Kaolin; Microscopy, Electron; Nerve Degeneration; Nerve Fibers, Myelinated; Nerve Regeneration; Neuroglia; Rabbits; Spinal Cord; Syringomyelia

The results of immunomorphologic and histochemical investigations of 12 rabbits with experimental syringomyelia are presented. Chronic pachymeningitis of the hind brain, resulting from the administration of kaolin leads to the disorders of liquor circulation on the level of outlet of the fourth ventricle this being a start mechanism for the cavity formation in the spinal cord. The reactive inflammatory, degenerative and immune reactions accompany the formation of cavity in the nervous tissue. The formation of cavity is followed by asymmetrical segment demyelination and reparative hyperplasia of the astroglial cells and gliosis of the cavity walls.

Topics: Animals; Inflammation; Kaolin; Nerve Degeneration; Nerve Regeneration; Nervous System; Rabbits; Syringomyelia